Overview

  • Product name

  • Description

    Rabbit polyclonal to FGFR2
  • Host species

    Rabbit
  • Tested applications

    Suitable for: IHC-P, ICC/IFmore details
  • Species reactivity

    Reacts with: Mouse, Human
  • Immunogen

    Synthetic peptide. This information is considered to be commercially sensitive.

  • Positive control

    • ICC/IF: U-2 OS cells. IHC-P: Mouse spleen and gallbladder tissue.

Properties

Applications

Our Abpromise guarantee covers the use of ab235277 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P 1/100. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.
ICC/IF Use a concentration of 5 µg/ml.

Target

  • Function

    Receptor for acidic and basic fibroblast growth factors.
  • Involvement in disease

    Defects in FGFR2 are the cause of Crouzon syndrome (CS) [MIM:123500]; also called craniofacial dysostosis type I (CFD1). CS is an autosomal dominant syndrome characterized by craniosynostosis (premature fusion of the skull sutures), hypertelorism, exophthalmos and external strabismus, parrot-beaked nose, short upper lip, hypoplastic maxilla, and a relative mandibular prognathism.
    Defects in FGFR2 are a cause of Jackson-Weiss syndrome (JWS) [MIM:123150]. JWS is an autosomal dominant craniosynostosis syndrome characterized by craniofacial abnormalities and abnormality of the feet: broad great toes with medial deviation and tarsal-metatarsal coalescence.
    Defects in FGFR2 are a cause of Apert syndrome (APRS) [MIM:101200]; also known as acrocephalosyndactyly type 1 (ACS1). APRS is a syndrome characterized by facio-cranio-synostosis, osseous and membranous syndactyly of the four extremities, and midface hypoplasia. The craniosynostosis is bicoronal and results in acrocephaly of brachysphenocephalic type. Syndactyly of the fingers and toes may be total (mitten hands and sock feet) or partial affecting the second, third, and fourth digits. Intellectual deficit is frequent and often severe, usually being associated with cerebral malformations.
    Defects in FGFR2 are a cause of Pfeiffer syndrome (PS) [MIM:101600]; also known as acrocephalosyndactyly type V (ACS5). PS is characterized by craniosynostosis (premature fusion of the skull sutures) with deviation and enlargement of the thumbs and great toes, brachymesophalangy, with phalangeal ankylosis and a varying degree of soft tissue syndactyly. Three subtypes of Pfeiffer syndrome have been described: mild autosomal dominant form (type 1); cloverleaf skull, elbow ankylosis, early death, sporadic (type 2); craniosynostosis, early demise, sporadic (type 3).
    Defects in FGFR2 are the cause of Beare-Stevenson cutis gyrata syndrome (BSCGS) [MIM:123790]. BSCGS is an autosomal dominant condition is characterized by the furrowed skin disorder of cutis gyrata, acanthosis nigricans, craniosynostosis, craniofacial dysmorphism, digital anomalies, umbilical and anogenital abnormalities and early death.
    Defects in FGFR2 are the cause of familial scaphocephaly syndrome (FSPC) [MIM:609579]; also known as scaphocephaly with maxillary retrusion and mental retardation. FSPC is an autosomal dominant craniosynostosis syndrome characterized by scaphocephaly, macrocephaly, hypertelorism, maxillary retrusion, and mild intellectual disability. Scaphocephaly is the most common of the craniosynostosis conditions and is characterized by a long, narrow head. It is due to premature fusion of the sagittal suture or from external deformation.
    Defects in FGFR2 are a cause of lacrimo-auriculo-dento-digital syndrome (LADDS) [MIM:149730]; also known as Levy-Hollister syndrome. LADDS is a form of ectodermal dysplasia, a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. LADDS is an autosomal dominant syndrome characterized by aplastic/hypoplastic lacrimal and salivary glands and ducts, cup-shaped ears, hearing loss, hypodontia and enamel hypoplasia, and distal limb segments anomalies. In addition to these cardinal features, facial dysmorphism, malformations of the kidney and respiratory system and abnormal genitalia have been reported. Craniosynostosis and severe syndactyly are not observed.
    Defects in FGFR2 are the cause of Antley-Bixler syndrome (ABS) [MIM:207410]. ABS is a multiple congenital anomaly syndrome characterized by craniosynostosis, radiohumeral synostosis, midface hypoplasia, malformed ears, arachnodactyly and multiple joint contractures. ABS is a heterogeneous disorder and occurs with and without abnormal genitalia in both sexes.
  • Sequence similarities

    Belongs to the protein kinase superfamily. Tyr protein kinase family. Fibroblast growth factor receptor subfamily.
    Contains 3 Ig-like C2-type (immunoglobulin-like) domains.
    Contains 1 protein kinase domain.
  • Cellular localization

    Secreted and Cell membrane.
  • Information by UniProt
  • Database links

  • Alternative names

    • bacteria-expressed kinase antibody
    • BBDS antibody
    • BEK antibody
    • BEK fibroblast growth factor receptor antibody
    • BFR1 antibody
    • CD332 antibody
    • CD332 antigen antibody
    • CEK3 antibody
    • CFD1 antibody
    • Craniofacial dysostosis 1 antibody
    • ECT1 antibody
    • FGF receptor antibody
    • FGFR 2 antibody
    • FGFR-2 antibody
    • Fgfr2 antibody
    • FGFR2_HUMAN antibody
    • Fibroblast growth factor receptor 2 antibody
    • Hydroxyaryl protein kinase antibody
    • Jackson Weiss syndrome antibody
    • JWS antibody
    • K SAM antibody
    • K-sam antibody
    • Keratinocyte growth factor receptor 2 antibody
    • Keratinocyte growth factor receptor antibody
    • KGFR antibody
    • KSAM antibody
    • protein tyrosine kinase, receptor like 14 antibody
    • soluble FGFR4 variant 4 antibody
    • TK14 antibody
    • TK25 antibody
    see all

Images

  • Formalin/PFA-fixed paraffin-embedded mouse gallbladder tissue stained for FGFR2 using ab235277 at a 1/100 dilution (30mins at RT). Secondary was an anti-rabbit poly-HRP IgG (Ready to use, 8 mins at RT).  Counterstained with hematoxylin. HIER using Citrate Buffer for 20mins.

  • U-2 OS (human bone osteosarcoma epithelial cell line) cells stained for FGFR2 using ab235277 at 5µg/ml (o/n at 4°C). Cells were fixed with 4% PFA and permeabilized using 0.3% Triton X-100.

    Counterstained with a Donkey anti-Rabbit IgG DyLight™ 488 conjugated preadsorbed secondary at 5µg/ml (1 h at RT).

  • Formalin/PFA-fixed paraffin-embedded mouse spleen tissue stained for FGFR2 using ab235277 at a 1/100 dilution (30mins at RT). Secondary was an anti-rabbit poly-HRP IgG (Ready to use, 8 mins at RT).  Counterstained with hematoxylin. HIER using Citrate Buffer for 20mins.

References

ab235277 has not yet been referenced specifically in any publications.

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